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Atlastin GTPase 1

SPG3A, atlastin, SPG3, ATL-1, FSP1
The protein encoded by this gene is a GTPase and a Golgi body transmembrane protein. The encoded protein can form a homotetramer and has been shown to interact with spastin and with mitogen-activated protein kinase kinase kinase kinase 4. This protein may be involved in axonal maintenance as evidenced by the fact that defects in this gene are a cause of spastic paraplegia type 3. Three transcript variants encoding two different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: spastin, HAD, CAN, SPG31, AGE
Papers using SPG3A antibodies
Caspase-3 inhibits growth in Saccharomyces cerevisiae without causing cell death
Vaux David L. et al., In The Journal of Cell Biology, 1998
... lines were made by transfecting NT2 cells with 2 μg of DNA linearized by digestion with Fsp1 (New England Biolabs, Inc.) ...
Papers on SPG3A
The Caenorhabditis elegans Werner syndrome protein participates in DNA damage checkpoint and DNA repair in response to CPT-induced double-strand breaks.
Ahn et al., Ulsan, South Korea. In Cell Signal, Jan 2016
We found that WRN-1 is involved in the checkpoint response to DSBs after CPT, inducing cell cycle arrest, is recruited to DSBs by RPA-1 and functions upstream of ATL-1 and ATM-1 for CHK-1 phosphorylation in the S-phase checkpoint.
Modeling of autosomal-dominant retinitis pigmentosa in Caenorhabditis elegans uncovers a nexus between global impaired functioning of certain splicing factors and cell type-specific apoptosis.
Cerón et al., Barcelona, Spain. In Rna, Dec 2015
Interestingly, RNAi of s-adRP genes produces an increase in the expression of atl-1 (homolog of human ATR), which is normally activated in response to replicative stress and certain DNA-damaging agents.
Tenascin-C, a Prognostic Determinant of Esophageal Squamous Cell Carcinoma.
Kim et al., Yanji, China. In Plos One, Dec 2015
The 5-year OS and DFS rates were remarkably lower in patients with positive expressions of both Tenascin-C and PDGFRα (p < 0.001), Tenascin-C and PDGFRβ (p < 0.001), Tenascin-C and SMA (p < 0.001), Tenascin-C and fibroblast activation protein (FAP) (p < 0.001), and Tenascin-C and fibroblast-stimulating protein-1 (FSP1) (p < 0.001) in ESCC stromal fibroblasts than in patients with negative expressions of both Tenascin-C and one of the abovementioned CAF markers.
[Primary culture and characteristics of colorectal cancer-associated fibroblasts].
Deng et al., Hangzhou, China. In Zhonghua Bing Li Xue Za Zhi, Oct 2015
qPCR showed that CAFs expressed more fibroblast activation protein (FAP) and less fibroblast specific protein 1 (FSP1) than that of NFs.
Hereditary spastic paraplegia SPG4: what is known and not known about the disease.
Baas et al., Philadelphia, United States. In Brain, Sep 2015
M1, due to its hydrophobic N-terminal domain not shared by M87, may insert into endoplasmic reticulum membrane, and together with reticulons, atlastin and REEP1, may play a role in the morphogenesis of this organelle.
Dasatinib Attenuates Pressure Overload Induced Cardiac Fibrosis in a Murine Transverse Aortic Constriction Model.
Kuppuswamy et al., Dublin, Ireland. In Plos One, 2014
Furthermore, dasatinib treatment inhibited NTK activation (primarily Pyk2 and Fak) and reduced the level of FSP1 positive cells in the PO myocardium.
Heterogeneity of collagen secreting cells in gingival fibrosis--an immunohistochemical assessment and a review of the literature.
BaniŢă et al., Craiova, Romania. In Rom J Morphol Embryol, 2014
AIM: In this work, we compared the histological features of the gingival lesions clinically diagnosed as fibrotic overgrowths due to various etiologic factors as well as an immunohistochemical assessment of fibroblasts phenotypic heterogeneity using the specific labeling for vimentin, α-smooth muscle actin (α-SMA) and fibroblast specific protein-1 (FSP1).
Mutation analysis of four Chinese families with pure hereditary spastic paraplegia: pseudo- X-linked dominant inheritance and male lethality due to a novel ATL1 mutation.
Jiang et al., Shenyang, China. In Genet Mol Res, 2014
Linkage analysis and ATL1 gene sequencing of amniocytes were performed for prenatal genetic diagnosis.
Endoplasmatic reticulum shaping by generic mechanisms and protein-induced spontaneous curvature.
Sackmann, Garching bei München, Germany. In Adv Colloid Interface Sci, 2014
They include atlastin, reticulon, REEP and the MT severing protein spastin.
[Hereditary spastic paraplegia: up to date].
Takiyama, Japan. In Rinsho Shinkeigaku, 2013
In 206 Japanese families with autosomal dominant HSP, SPG4 was the most common form, accounting for 38%, followed by SPG3A (5%), SPG31 (5%), SPG10 (2%), and SPG8 (1%).
The global epidemiology of hereditary ataxia and spastic paraplegia: a systematic review of prevalence studies.
Coutinho et al., Feira, Portugal. In Neuroepidemiology, 2013
The most common AD-HSP form in every population was spastic paraplegia, autosomal dominant, type 4 (SPG4), followed by SPG3A, while SPG11 was the most frequent AR-HSP, followed by SPG15.
Atl1 regulates choice between global genome and transcription-coupled repair of O(6)-alkylguanines.
Margison et al., Manchester, United Kingdom. In Mol Cell, 2012
Data show that alkyltransferase-like 1 (Atl1)can play a pivotal role in selecting a specific nucleotide excision repair (NER) pathway, depending on the nature of the DNA modification.
ER network formation requires a balance of the dynamin-like GTPase Sey1p and the Lunapark family member Lnp1p.
Ferro-Novick et al., San Diego, United States. In Nat Cell Biol, 2012
Although studies on endoplasmic reticulum (ER) structure and dynamics have focused on the ER tubule-forming proteins (reticulons and DP1/Yop1p) and the tubule fusion protein atlastin, nothing is known about the proteins and processes that act to counterbalance this machinery.
GTP-dependent packing of a three-helix bundle is required for atlastin-mediated fusion.
Daga et al., Conegliano, Italy. In Proc Natl Acad Sci U S A, 2011
increasing the distance of atlastin complex formation from the membrane inhibits fusion, suggesting that this distance is crucial for atlastin to promote fusion
Structures of the atlastin GTPase provide insight into homotypic fusion of endoplasmic reticulum membranes.
Hu et al., Tianjin, China. In Proc Natl Acad Sci U S A, 2011
experiments also show that membrane fusion is facilitated by the C-terminal cytosolic tails following the two transmembrane segments. Finally, our results show that mutations in ATL1 causing hereditary spastic paraplegia compromise homotypic ER fusion
Hereditary spastic paraplegia associated with axonal neuropathy: a novel mutation of SPG3A in a large family.
Yoon et al., Toronto, Canada. In J Clin Neuromuscul Dis, 2011
We identified a novel mutation, c.1040T>C (p. M347T), in a family with axonal neuropathy in addition to spastic paraplegia.
Structural basis for the nucleotide-dependent dimerization of the large G protein atlastin-1/SPG3A.
Sondermann et al., Ithaca, United States. In Proc Natl Acad Sci U S A, 2011
a model for nucleotide-dependent regulation of atlastin with implications for membrane fusion. This mechanism is affected in several mutants associated with HSP, providing insights into disease pathogenesis.
Homotypic fusion of ER membranes requires the dynamin-like GTPase atlastin.
Daga et al., Conegliano, Italy. In Nature, 2009
Here we demonstrate that Drosophila Atlastin--the fly homologue of the mammalian GTPase atlastin 1 involved in hereditary spastic paraplegia--localizes on ER membranes and that its loss causes ER fragmentation.
A class of dynamin-like GTPases involved in the generation of the tubular ER network.
Blackstone et al., Boston, United States. In Cell, 2009
Since atlastin-1 mutations cause a common form of hereditary spastic paraplegia, we suggest ER-shaping defects as a neuropathogenic mechanism.
Mutations in a newly identified GTPase gene cause autosomal dominant hereditary spastic paraplegia.
Fink et al., Ann Arbor, United States. In Nat Genet, 2001
Eight autosomal dominant HSP (ADHSP) loci have been identified, the most frequent of which is that linked to the SPG4 locus on chromosome 2p22 (found in approximately 42%), followed by that linked to the SPG3A locus on chromosome 14q11-q21 (in approximately 9%).
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